Figure 5.

Pretreatment of mice with KCC2 activators prevents the development of BDZ-RSE

(A) Line diagram outlining the experimental design.

(B) Exemplar EEG traces are shown for mice injected with V (s.c.) 2 h prior to dosing i.p. with 20 mg/kg KA. 2 h following KA injection, mice were dosed i.p. with 5 mg/kg DZ, and EEG recordings were extended for a further 1 h. The lower trace represents an enlargement of the green bar indicated in the upper trace.

(C) Exemplar EEG traces are shown for mice injected with 50 mg/kg 2 h prior to dosing i.p. with 20 mg/kg KA. 2 h following KA injection, mice were dosed i.p. with 5 mg/kg DZ, and EEG recordings were extended for a further 1 h. The lower trace represents an enlargement of the green bar indicated in the upper trace.

(D) The time to the first seizure, the onset of SE, and the percentage of total time in epileptiform activity were compared between treatment groups (n = 9 mice).

(E) EEG recordings were subjected to FFT, and spectral plots are shown for frequencies between 1 and 100 Hz for mice treated with V or 350 2 h after KA injection. Total EEG power was then compared between treatments (n = 9 mice).

(F) EEG recordings from mice pretreated with V 2 h following KA injection and 10 min after dosing with DZ were subjected to FFT, and spectral plots are shown for frequencies between 1 and 100 Hz. Total EEG power was then compared (n = 9 mice).

(G) EEG recordings from mice pretreated with 350 2 h following KA injection and 10 min after dosing with DZ were subjected to FFT, and spectral plots are shown for frequencies between 1 and 100 Hz. Total EEG power was then compared between treatments (n = 9 mice).

In all panels, p values were determined using t tests, ∗p < 0.05.